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Shu-wen W Chen

Publications and source records attributed to Shu-wen W Chen.

3 recordsLinked to original sources

Multi-template approach to modeling engineered disulfide bonds.

The key issue for disulfide bond engineering is to select the most appropriate location in the protein. By surveying the structure of experimentally engineered disulfide bonds, we found about half of them that have geometry incompatible with any native disulfide bond geometry. To improve the current prediction methods that tend to apply either ideal geometrical or energetical criteria to single three-dimensional structures, we have combined a novel computational protocol with the usage of multiple protein structures to take into account protein backbone flexibility. The multiple structures can be selected from either independently determined crystal structures for identical proteins, models of nuclear magnetic resonance experiments, or crystal structures of homology-related proteins. We have validated our approach by comparing the predictions with known disulfide bonds. The accuracy of prediction for native disulfide bonds reaches 99.6%. In a more stringent test on the reported engineered disulfide bonds, we have obtained a success rate of 93%. Our protocol also determines the oxido-reduction state of a predicted disulfide bond and the corresponding mutational cost. From the energy ranking, the user can easily choose top predicted sites for mutagenesis experiments. Our method provides information about local stability of the engineered disulfide bond surroundings.

Bacterial Proteins↗

Model of a ternary complex between activated factor VII, tissue factor and factor IX.

Upon binding to tissue factor, FVIIa triggers coagulation by activating vitamin K-dependent zymogens, factor IX (FIX) and factor X (FX). To understand recognition mechanisms in the initiation step of the coagulation cascade, we present a three-dimensional model of the ternary complex between FVIIa:TF:FIX. This model was built using a full-space search algorithm in combination with computational graphics. With the known crystallographic complex FVIIa:TF kept fixed, the FIX docking was performed first with FIX Gla-EGF1 domains, followed by the FIX protease/EGF2 domains. Because the FIXa crystal structure lacks electron density for the Gla domain, we constructed a chimeric FIX molecule that contains the Gla-EGF1 domains of FVIIa and the EGF2-protease domains of FIXa. The FVIIa:TF:FIX complex has been extensively challenged against experimental data including site-directed mutagenesis, inhibitory peptide data, haemophilia B database mutations, inhibitor antibodies and a novel exosite binding inhibitor peptide. This FVIIa:TF:FIX complex provides a powerful tool to study the regulation of FVIIa production and presents new avenues for developing therapeutic inhibitory compounds of FVIIa:TF:substrate complex.

Algorithms↗

Structural basis for preferential binding of non-ortho-substituted polychlorinated biphenyls by the monoclonal antibody S2B1.

Polychlorinated biphenyls (PCBs) are a family of 209 isomers (congeners) with a wide range of toxic effects. In structural terms, they are of two types: those with and those without chlorines at the ortho positions (2, 2', 6 and 6'). Only 20 congeners have no ortho chlorines. Three of these are bound by the aryl hydrocarbon receptor and are one to four orders of magnitude more toxic than all others. A monoclonal antibody, S2B1, and its recombinant Fab have high selectivity and nanomolar binding affinities for two of the most toxic non-ortho-chlorinated PCBs, 3,4,3',4'-tetrachlorobiphenyl and 3,4,3',4',5'-pentachlorobiphenyl. To investigate the basis for these properties, we built a three-dimensional structure model of the S2B1 variable fragment (Fv) based on the high-resolution crystallographic structures of antibodies 48G7 and N1G9. Two plausible conformations for the complementarity-determining region (CDR) H3 loop led to two putative PCB-binding pockets with very different shapes (models A and B). Docking studies using molecular mechanics and potentials of mean force (PMF) indicated that model B was most consistent with the selectivity observed for S2B1 in competition ELISAs. The binding site in model B had a deep, narrow pocket between V(L) and V(H), with a slight constriction at the top that opened into a wider pocket between CDRs H1 and H3 on the antibody surface. This binding site resembles those of esterolytic antibodies that bind haptens with phenyl rings. One phenyl ring of the PCB fits into the deep pocket, and the other ring is bound in the shallower one. The bound PCB is surrounded by the side chains of TyrL91, TyrL96 and TrpH98, and it has a pi-cation interaction with ArgL46. The tight fit of the binding pocket around the ortho positions of the bound PCBs indicates that steric hindrance of ortho chlorines in the binding site, rather than induced conformational change of the PCBs, is responsible for the selectivity of S2B1.

Amino Acid Sequence↗